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Journal of Virology, June 2009, p. 6039-6047, Vol. 83, No. 12
0022-538X/09/$08.00+0     doi:10.1128/JVI.00135-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

JNK and p38 Mitogen-Activated Protein Kinase Pathways Contribute to Porcine Circovirus Type 2 Infection{triangledown}

Li Wei,1 Zhongwu Zhu,2 Jing Wang,1 and Jue Liu1*

Institute of Animal Husbandry and Veterinary Medicine, Beijing Municipal Academy of Agriculture and Forestry Sciences, No. 9 Shuguang Garden Central Road, Haidian District, Beijing 100097,1 Hunan Entry-Exit Inspection and Quarantine Bureau, No. 188 Xiangfu Road, Changsha 410003, People's Republic of China2

Received 21 January 2009/ Accepted 23 March 2009

Infection with a wide variety of viruses often perturbs host cell signaling pathways including the Jun NH2-terminal kinase/stress-activated kinase (JNK/SAPK) and the p38 mitogen-activated protein kinase (p38/MAPK), which are important components of cellular signal transduction pathways. The present study demonstrated for the first time that porcine circovirus type 2 (PCV2), which is the primary causative agent of an emerging swine disease, postweaning multisystemic wasting syndrome, can activate JNK1/2 and p38 MAPK pathways in PCV2-infected PK15 cells. However, PCV2 at an early stage of infection, as well as UV-irradiated PCV2, failed to activate these two MAPK families, which demonstrated that PCV2 replication was necessary for their activation. We further found that PCV2 activated the phosphorylation of JNK1/2 and p38 MAPK downstream targets c-Jun and ATF-2 with virus replication in the cultured cells. The roles of these kinases in PCV2 infection were further evaluated using specific inhibitors: the JNK inhibitor 1 for JNK1/2 and SB202190 for p38. Inhibition of JNK1/2 and p38 kinases by these specific inhibitors did result in significant reduction of PCV2 viral mRNA transcription and protein synthesis, viral progeny release, and blockage of PCV2-induced apoptotic caspase-3 activation in the infected cells. Taken together, these data suggest that JNK/SAPK and p38 MAPK pathways play important roles in the PCV2 replication and contribute to virus-mediated changes in host cells.

* Corresponding author. Mailing address: Institute of Animal Husbandry and Veterinary Medicine, Beijing Municipal, Academy of Agriculture and Forestry Sciences, No. 9 Shuguang Garden Central Road, Haidian District, Beijing 100097, People's Republic of China. Phone: 86-10-51503548. Fax: 86-10-88433070. E-mail: liujue{at}263.net

{triangledown} Published ahead of print on 1 April 2009.

Journal of Virology, June 2009, p. 6039-6047, Vol. 83, No. 12
0022-538X/09/$08.00+0     doi:10.1128/JVI.00135-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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